Endopelvic fascia treatment for incontinence

ABSTRACT

Methods, devices, and systems for treating the support structures of the body, particularly for incontinence, take advantage of two mechanisms to enhance the support provided by the fascia, ligaments and tendons: first, the invention increases a modulus of elasticity of these tissues, and particularly of the fascial tissues. The increase in modulus can be effected by directing sufficient energy to the fascial tissue so as to promote the formation of scar tissue. The second mechanism attaches tissue planes together, often by directing energy to an interface between adjacent fascial tissues.

CROSS-REFERENCES TO RELATED APPLICATIONS

This application is a continuation of U.S. patent application Ser. No.09/413,100 filed Oct. 6, 1999 is now U.S. Pat. No. 6,292,700, and claimsthe benefit and priority of U.S. Provisional Patent Application No.60/153,330 filed Sep. 10, 1999, the full disclosures of which areincorporated herein by reference for all purposes.

BACKGROUND OF THE INVENTION

1. Field of the Invention

The present invention generally relates to medical devices, methods, andsystems, particularly for the treatment of urinary incontinence.

Urinary incontinence arises in both men and women with varying degreesof severity, and from different causes. In men, the condition frequentlyoccurs as a result of prostatectomies which result in mechanical damageto the urinary sphincter. In women, the condition typically arises afterpregnancy when musculoskeletal damage has occurred as a result ofinelastic stretching of the structures supporting the genitourinarytract. Specifically, pregnancy can result in inelastic stretching of thepelvic floor, the external sphincter, and the tissue structures whichsupport the bladder, urethra, and bladder neck region. In each of thesecases, urinary leakage typically occurs when a patient's abdominalpressure increases as a result of stress, e.g., coughing, sneezing,laughing, exercise, or the like.

Treatment of urinary incontinence can take a variety of forms. Mostsimply, the patient can wear absorptive devices or clothing, which isoften sufficient for minor leakage events. Alternatively oradditionally, patients may undertake exercises intended to strengthenthe muscles in the pelvic region, or may attempt a behavior modificationintended to reduce the incidence of urinary leakage.

In cases where such non-interventional approaches are inadequate orunacceptable, the patient may undergo surgery to correct the problem. Awide variety of procedures have been developed to correct urinaryincontinence in women. Several of these procedures are specificallyintended to support the bladder neck region. For example, sutures,straps or other artificial structures are often looped around thebladder neck and affixed to the pelvis, the endopelvic fascia, theligaments which support the bladder, or the like. Other proceduresinvolve surgical injections of bulking agents, inflatable balloons, orother elements to mechanically support the bladder neck.

In work done related to the present invention, it has been proposed totreat urinary incontinence by selectively contracting or shrinking aportion of the pelvic support tissue so as to reposition the bladderand/or urogenital tract. U.S. patent application Ser. No. 08/910,370generally describes laparoscopic and other minimally invasive devices,methods, and systems for shrinking tissues, particularly for treatmentof incontinence. U.S. patent application Ser. No. 09/133,496 describesnoninvasive devices, methods, and systems for shrinking of tissues,often by cooling a surface of an intermediate tissue and directingenergy through the cooled intermediate tissue to the target tissue so asto effect shrinkage. U.S. patent application Ser. No. 09/170,767 isdirected to static devices and methods to shrink tissues forincontinence. Finally, U.S. patent application Ser. No. 09/103,352describes tuck and fold fascia shortening for incontinence. Each ofthese applications is assigned to the present assignee, and their fulldisclosures are incorporated herein by reference.

While these recent proposals for treatment of incontinence representsignificant advancements in the art, treatment of incontinence and otherconditions related to insufficient tissue support could benefit fromstill further advances. In particular, it is generally beneficial tominimize collateral damage imposed on the treated and adjacent tissuesduring any therapy. It would further be beneficial to providealternative treatment mechanisms for reducing or eliminating theseverity and occurrence of incontinence events.

A variety of other problems can arise when tissues of the body fail toprovide adequate support. Weakened pelvic support tissues (particularlythe ligaments and fascia of the pelvic area) can lead to a variety ofailments including, for example, cystocele, prolapse, and the like.Cosmetic surgeries are also often performed to enhance the supportprovided by fascial tissues. For example, abdominoplasty (often called a“tummy tuck”) is often performed to enhance support provide by theabdominal wall. The distortion of these support tissues may be due tostrain, advanced age, congenital predisposition, or the like.

For these reasons, it would be desirable to provide improved devices,methods, and systems for treating the support tissues of the body. Itwould be particularly desirable to provide techniques for treatment ofincontinence and other conditions by enhancing the support of the body'sown tissue systems. It would further be advantageous if these improvedtechniques could take advantage of the recent advancements in minimallyinvasive and noninvasive therapies described hereinabove, and couldeffect treatment with decreased collateral damage. Some or all of theseadvantages are provided by the invention described hereinbelow.

2. Description of the Background Art

U.S. patent application Ser. Nos. 08/910,370; 09/133,496; 09/170,767;and 09/103,352 are described hereinabove. PCT Application No. 97/43,971describes a method and apparatus for ablating turbinates. PCTApplication No. 98/38,936 describes a method and apparatus for treatingvenous insufficiency. The impact of surgical treatments of the urethrawere described by Shlomo Raz in FEMALE UROLOGY, 2^(nd) Ed. (1996). Thisreference also describes techniques of surgical repair for treatment ofcystocele on pages 340-342, while various alternative known surgicalinterventions for treatment of incontinence are schematicallyillustrated on page 356. At least some of these procedures are alsodescribed in FEMALE PELVIC DISORDERS, INVESTIGATION AND MANAGEMENT by J.Thomas Benson (1992) on pages 239-240.

An electrosurgical probe for the controlled contraction of tissues ofjoints and for dermatological indications is described in U.S. Pat. No.5,458,596. A bipolar electrosurgical probe having electrodes formed overa restricted arc of its distal end for treatment of, for example, theesophagus, is described in U.S. Pat. No. 4,765,331. Systems and methodsfor electrosurgical cutting and ablation are described in U.S. Pat. No.5,697,882. Methods and apparatus for controlled contraction of softtissues is described in U.S. Pat. No. 5,569,242. U.S. Pat. No. 5,423,811describes a method for RF ablation using cooled electrodes.

SUMMARY OF THE INVENTION

The present invention provides improved methods, devices, and systemsfor treating the support structures of the body, as a treatment forincontinence and other conditions. In general, the invention takesadvantage of two mechanisms to enhance the support provided by thefascia, ligaments and tendons: first, the invention increases a modulusof elasticity of these tissues, and particularly of the fascial tissues.The increase in modulus can be effected by directing sufficient energyto the fascial tissue so as to promote the formation of scar tissue. Theresulting scarred tissue is generally significantly less elastic thanthe original fascia, and may also have an increased thickness (either asthe result of fascial shrinkage or from the proliferation of scar tissueand/or smooth muscle cells). This local increase in modulus of thescarred support tissue can transfer stress and strain from the area oftreatment to adjoining areas, and may also shorten the response time ofthe tissue plane to stress pulses (such as those which might result inincontinence events).

The second mechanism encompassed by the invention for enhancing thesupport is to promote attachment of adjacent support tissues to eachother. Adjacent fascial tissue surfaces in the pelvic support system areoften able to slide freely against each other. This free lateralmovement allows the visceral organs to expand and contract over time.However, if there is inadequate support, the motion may become extremeand result in incontinence, prolapse, and other conditions. By directingenergy (for example) at the interface between sliding fascial tissuesurfaces, the relative motion at the interface can be restricted so asto enhance support of the pelvic viscera. Heating may be used to induceacute (through tissue fusion) and/or chronic (through the growth ofcross-linked collagenated tissue or adhesions) attachments between thetissues.

In a first aspect, the invention provides a method for treatingincontinence. The method comprises reducing an elasticity of a pelvicsupport tissue system sufficiently so that the tissue system inhibitsincontinence. Generally, the elasticity will be reduced by promotingscarring of fascia supporting the urethra and/or bladder. The scarringreduces the modulus of elasticity of the fascial tissue so that thefascial tissue inhibits incontinence. Such scarring will preferably bepromoted by directing energy into the fascial tissue so as to injure thefascial tissue without ablating the fascial tissue. While such energycan be delivered in the form of ultrasound, microwave, laser, or thermalconduction, it will preferably be in the form of an RF current conductedthrough the tissue so that the tissue's impedance effects heating.

Advantageously, heating the fascial tissue to a temperature of about 45°C. or more is sufficient to promote the formation of scar tissue andthereby decrease elasticity. Hence, elasticity can be reduced by heatingthe tissue below the temperatures generally used to effect contractionor shrinkage (typically over about 60° C.). These lower tissuetemperatures can significantly reduce collateral damage, particularlywhere the elasticity of the tissue is reduced without significantshrinkage. As elasticity reduction and shrinking represent two distinctstructural alterations in the tissue system, they may be appliedindependently or in selective combinations so as to provide the desiredchange in structural support.

Typically, the elasticity of the tissue is reduced along a length oftissue. The tissue will be susceptible to loading along this length byan incontinence-event stress such as coughing, laughing, exercise, orthe like. Reduction in the elasticity may be provided with or withoutselective reduction in the length (typically by collagenous tissueshrinkage). The present invention allows selective tailoring of anincontinence therapy in response to a comparison between a change inurethral pressure relative to a change in vesical pressure during anincontinence event stress pulse.

A variety of tissues and tissue structures may be targeted for thepresent incontinence treatments. These include the tissue structures andsystems of the pelvic floor and/or diaphragm, bladder and urethra,vagina, uterus, bowel, and the like. Treatment modalities includethermal, electrosurgical, laser, focused ultrasound or microwave, and avariety of bioactive or biochemical agents including local drugdelivery, caustic compounds, pleurodesis agents, sclerosing agents,growth factors, surgical sealants, and/or the like. When bioactiveagents are used, the invention may employ any of a wide variety ofavailable compounds being marketed.

In another aspect, the invention provides a method for treatingincontinence. The method comprises promoting attachment between a firsttissue and second tissue with energy or an active agent. The secondtissue slidingly engages the first tissue prior to attachment, so thatthe attachment limits motion between the first and second tissues. Thelimited relative motion of these tissues inhibits incontinence.

Preferably, the attachment promoting step comprises directing sufficientenergy to an interface between the first tissue and second tissue toinjure a fascial tissue surface without ablating the fascial tissue. Theinvention encompasses a variety of energy directing mechanisms, with thepreferred energy comprising RF current transmitted to the fascialtissue. Typically, first and second fascial tissue surfaces of the firstand second tissue will be heated. The heat may acutely fuse the tissuesurfaces together. Optionally, collagen of the first and second tissueswill be cross-linked during the healing process. In other embodiments,the attachment promoting step may result in the formation of adhesionsbetween the first and second tissues. Surprisingly, although theprevention of adhesion formation is an important goal of many pelvicsurgeries, controlled adhesion generation may result in significantpatient benefit where the adhesion serves to enhance the support of thepelvic viscera.

In another aspect, the invention provides a method for treatingincontinence. This method comprises measuring a urethral pressure and avesicle pressure during a stress. A change in the measured urethralpressure is compared relative to a change in the measured vesiclepressure. An elasticity of a pelvic support system is reduced inresponse to the comparing step sufficiently that the urethral pressurewill remain greater than the vesicle pressure during stress.

In yet another aspect, the invention provides a system to treatincontinence. The system comprises a probe for delivering energy or anactive agent to a pelvic support tissue so as to reduce an elasticity ofthe pelvic support tissue. A control system is coupled to the probe. Thecontrol system limits the delivery from the probe to avoid collateraldamage.

In many embodiments, the control system will limit an amount of theenergy or the agent to avoid shrinkage of the tissue. The probe willpreferably comprise an energy delivery member, ideally comprising an RFelectrode. The exemplary system further includes a urethral pressuresensor, a vesicle pressure sensor, and a processor coupled to theurethral and vesicle pressure sensors. The processor generates an outputindicating a change in urethral pressure relative to a change in vesiclepressure. This output is particularly useful for determining the desiredreduction in elasticity of the pelvic support tissue.

In another aspect, the invention provides a kit for treatingincontinence. The kit comprises a probe for directing energy or abioactive agent to a pelvic tissue system. Instructions for using theprobe will describe methods for enhancing structural support provided bythe tissue system so that incontinence is inhibited. The instructionsand probe may be packaged together, and the method steps of theinstructions may be any of the methods described herein.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a schematic illustration of a diagnosis and treatment systemfor urinary incontinence, according to the principles of the presentinvention.

FIG. 2 is a cross-sectional view illustrating some of the pelvic supporttissues which may be targeted for treatment by the system of FIG. 1.

FIG. 3 is a schematic cross-sectional view illustrating how anexcessively elastic pelvic support system can discharge when subjectedto a pressure pulse.

FIGS. 4A and B are alternative schematic illustrations showing howexcessive elasticity of the pelvic support system can delay sealingforces against the urethra, thereby contributing to incontinence.

FIG. 5 is a cross-section view through an endopelvic fascia layer whichhas been treated according to the principles of the present invention toreduce the elasticity of the pelvic support system.

FIGS. 6A-C illustrate an alternative mechanism for enhancing thestructural support of the pelvic support system by attaching two layersof endopelvic fascia which normally slide against each other.

FIGS. 7A-C illustrate a static tissue treatment probe for reducing theelasticity and/or fusing fascial tissues using radio frequency energy,and methods for its use.

FIGS. 8A and B illustrate an alternative probe and method for its use toreduce the elasticity of endopelvic fascia by promoting the formation ofscar tissue, and/or for promoting the attachment of two fascial layerstogether.

FIG. 9 is a cross-sectional drawing showing a noninvasive probedirecting radio frequency current through a cooled intermediate tissueso as to promote the formation of scar tissue along an endopelvic fascialayer.

FIG. 10 is a graphical output showing a change in urethral pressurerelative to a change in vesicular pressure for determine a desiredchange in elasticity of a pelvic support system.

FIG. 11 schematically illustrates a kit including a probe andinstructions for its use to enhance the support of a tissue supportsystem by reducing a modulus of elasticity of a support tissue, and/orby affixing adjacent support tissues together.

DESCRIPTION OF THE SPECIFIC EMBODIMENTS

The present invention generally provides methods, devices, and systemswhich enhance the structural support provided by a body's tissues,particularly as a therapy for incontinence. The techniques of theinvention will generally involve promoting the formation of scar tissueso as to stiffen a tissue structure, and/or the attachment of twoadjacent tissues (which are normally free to slide relative to eachother) to each other. Energy may be directed from a probe into one ormore fascial tissues of the pelvic support system. The energy may leadto the formation of stiff scar tissue, and/or it may attach adjacentfascial tissues together by fusing, cross-linking of collagen, theformation of adhesions, or the like. Optionally, the energy may alsocause contraction of the fascial tissue by heating this collagenouslayer to a contraction temperature over about 60° C. Alternatively,stiffening and/or attachment of adjacent fascial layers may be providedwithout significant contraction, as scar tissue can be promoted byheating the fascia to temperature below that at which significantcontraction takes place, for example, over about 45° C.

As these techniques will be effective for controllably and repeatablyenhancing the structural support of a wide variety of fascia and othercollagenous tissues through the body, they will find applications in awide variety of therapies, including cosmetic applications, orthopedicapplications, treatment of hernias, and the like. However, the mostimmediate application for the invention will be to enhance a tissuesystem's support of the bladder, bladder neck region, and urethra so asto inhibit urinary incontinence, generally without sutures, slings,fasteners, or other artificial structures.

The techniques of the present invention will often be used to stiffen orattach fascia, tendons, and other collagenous tissues, preferablywithout ablation of these collagenous tissues. As used herein, thismeans that collagenous tissues are not removed and their function(particularly their structural support function) is not destroyed.Histologically, some tissue necrosis may occur, and the structuralstrength of the tissues may initially decrease immediately aftertreatment. Nonetheless, the treated tissues will generally continue toprovide at least some structural support, and their structural strengthshould increase during the healing process so that the healed tissue haspreferably the same ultimate structural strength as, and often greaterstiffness (for example, having a higher modulus of elasticity so as tostretch less under tension) than before treatment.

Referring now to FIG. 1, a urinary incontinence diagnosis and treatmentsystem 10 generally includes a diagnostic subsystem 12 for diagnosingstress incontinence and a treatment subsystem 14 which provides atherapy for a specific patient in response to a specific diagnosis.Diagnostic system 12 generally includes a catheter 16 for sensingpressures in bladder B and in urethra U, and a holder 18 which helpskeep the catheter in position when the bladder and urethra move during apressure pulse. Signals from catheter 16 are transmitted to processor20, which displays a pressuregram 22 on display 24. Pressuregram 22indicates a change in urethral pressure relative to a change invesicular pressure.

Diagnostic system 12 is described more fully in co-pending U.S. patentapplication Ser. No. 09/288,865, filed on Mar. 9, 1999, and inProvisional Application No. 60/104,818, filed on Oct. 19, 1998, the fulldisclosures of which are incorporated by reference. In general, catheter16 includes pressure sensors 26. Pressure sensors 26 sense vesicularpressure within bladder B, and sense a maximum urethral pressure withinurethra U, with the location of this maximum urethral pressure sometimesbeing referred to as the mid-urethra MU. To maintain the location ofcatheter 16 during a pressure pulse, holder 18 supports the catheterwhile allowing the catheter to move with the external meatus EM.

To maintain the position of catheter 16 within urethra U, the cathetermay include a balloon which generally engages the surrounding urethra,or holder 18 may include a surface which engages, and which supports thecatheter relative to, the external meatus EM. This allows catheter 16 toprovide pressure signals which accurately reflect the urethral andvesicular pressure throughout a pressure pulse, which may be induced byhaving a patient cough, by applying an external impulse against thepatient's abdomen, or the like. Processor 20 can record these pressuresthroughout multiple pressure pulses for displaying as pressuregram 22.Generally, where urethral pressure remains higher than vesicularpressure (above the P_(u)=P_(v) line on the pressuregram) leakage willnot occur. However, where vesicular pressure increases faster thanurethral pressure during a pressure pulse, a sufficiently strong pulsemay produce leakage.

To increase the rate of change of the urethral pressure for eachincrement of change in the vesicular pressure, treatment system 14 maybe employed to increase a modulus of the patient's pelvic supportsystem. Often, treatment system 14 will selectively promote formation ofscar tissue along a fascial plane. Some of the components of treatmentsystem 14 are substantially similar to those of the system described inco-pending U.S. patent application Ser. No. 09/170,767, the fulldisclosure of which is incorporated herein by reference. To remodeltissues of the pelvic support system, power supply 26 directs RF currentto selected pairs of electrodes on probe 28 under the direction ofprocessor 20. Here, selective heating commands from processor 20 areimplemented by a separate switching unit 29. It should be understoodthat in alternative arrangements, the switching unit may be incorporatedinto processor 20, power supply 26, or probe 28, and that separateprocessors may be provided for the diagnostic and treatment subsystems.In many embodiments, feedback on the course of treatment will beprovided in the form of feedback signals FS transmitted from probe 28 toprocessor 20.

The tissues of the pelvic support system, which generally maintains theposition of much of the genitourinary tract, and in particular theposition of urinary bladder B and urethra U, are illustrated in FIG. 2.In general, endopelvic fascia EF may define a hammock-like structurewhich extends laterally between the left and right arcus tendinousfascia pelvis ATFP. These lateral structures may extend substantiallybetween the anterior and posterior portions of the pelvis, so that theendopelvic fascia EF largely defines the pelvic floor.

The fascial tissue of the pelvic floor may comprise tissues referred tounder different names by surgeons of different disciplines, and possiblyeven by different practitioners within a specialty. In fact, somesurgeons may assign a collagenous support structure of the endopelvicfascia one name when viewed from a superior approach, and a differentname when viewed from an inferior approach. Some of the endopelvicfascia may comprise two collagenous layers with a thin muscular layertherebetween, or may comprise a single collagenous layer. Thehammock-like endopelvic fascia described herein may be damaged ormissing, particularly after pregnancy, so that the support of thegenitourinary tract is instead provided by a variety of fascial layers,muscular tissues, ligaments, and/or tendons within the pelvis. Hence,the treatment of the present invention may be directed at a variety oftissue structures defining the pelvic floor and/or diaphragm (including:anterior sacro-coccygeal ligament; arcus tendineus fasciae pelvis ATFP,the white line of the pelvis; fasciae of the obturator internus muscle;the arcus tendineus levator ani or “picket fence” to the iliococcygeusportion of the levator ani muscle; bulbocavemosus muscle;ischiocavemosus muscle; urethrovaginal sphincter; m. compressor urethraemuscle; and m. sphincter urethrovaginal muscle which replaces deepperineal muscle); structures of the bladder and urethra (including:urethrovesical fascia; detrusor muscle; and the pubo-coccygeus musclewhich relaxes to open the bladder neck, initiating micturation);structures of the vagina (including: vagino-uterine fascia, laminapropria—the dense connective tissue layer just under the epithelium;pubo-urethral or puboprostatic ligaments; pubo-vesicle ligament andposterior pubo-urethral or puboprostatic ligament; pubovesicle muscle, asmooth muscle that is integrated with the pubovesicle ligament; andpubocervical fascia which attaches to the ATFP); structures of theuterus (including: round ligament; sacrouterine ligament; and broadligament); and structures of the bowel (including: rectal fascia andmackenrodt's ligament).

The effects of excessive elasticity of the pelvic support tissues areillustrated in FIGS. 3, 4A and 4B. In FIG. 3, a pressure pulse P movesbladder B from an initial position 30 to a lowered position as shown. Asendopelvic fascia EF stretches excessively in this case, the fluidpressure within the bladder advances into the bladder neck and downurethra U. Leakage may result in part because the endopelvic fasciaallows the bladder to drop below its initial position, at which fluidpressure within the bladder actually helps to seal the bladder neck.Perhaps even more importantly, stretching of the endopelvic fascia mayalter the timing of pressure pulse transmission to urethra U.

When a continent woman coughs, the pressure in the urethra will oftenincrease more than one-tenth of a second prior to the increase inbladder pressure. In women with stress incontinence, the bladderpressure may rise first. The effect of a stretched endopelvic fascia onthis difference in timing can be understood with reference to FIGS. 4Aand B.

FIG. 4A schematically illustrates a simplified theoretical pelvicsupport system for a woman with stress incontinence. When pressure pulseP first begins to act on urethra U, the bladder, bladder neck, andurethra are disposed at initial position 30. As endopelvic fasciastretches significantly under the effects of pressure pulse P, there isa significant time delay between initiation of the pressure pulse andtransmission of a closing force against urethra U. For example, urethraU may be closed by transmission of pressure pulse P between one-tenthand one-half second after pulse is imposed on the bladder. Hence,leakage would occur during this time delay.

This situation is different for a continent woman having the simplifiedtheoretical pelvic support system illustrated in FIG. 4B. In this case,endopelvic fascia EF stretches much less under the influence of pressurepulse P, so that the time delay between initiation of the pressure pulseand transferring sufficient force to urethra U to effect closure issignificantly less. More specifically, an increase in the modulus ofelasticity of the endopelvic fascia and the pelvic support systemshortens the response time of the tissue system to momentary stress. Bytreating the endopelvic fascia to increase its stiffness, the decenttime of the pelvic viscera during a cough will be much shorter than anuntreated, highly elastic tissue.

It should be noted that the continent woman's support structureschematically illustrated in FIG. 4B has an initial position 30′ inwhich the endopelvic fascia EF is more taut than the incontinent woman'sstructure illustrated in FIG. 4A. In other words, excessive length ofthe pelvic support tissues may add to the delay and bladder movement,independently of the effects of excessive elasticity. Hence, in manycases, it will be beneficial to both increase the modulus of theendopelvic fascia and decrease its length so as to improve continence.Advantageously, the collagenous fascial tissues may be selectivelycontracted using many of the same system components described herein,often by heating this collagenous tissue to a slightly highertemperature than that used to promote scar tissue formation. Systems andmethods for selectively contracting endopelvic fascia and othercollagenous support structures are described more fully in co-pendingU.S. patent application Ser. Nos. 09/133,496 and 08/910,370, previouslyincorporated herein by reference.

Referring now to FIG. 5, a selective target region 32 of endopelvicfascia EF has been treated to enhance a modulus of elasticity of theendopelvic fascia, and thereby of the pelvic support system. Theincrease in modulus of the fascial tissue may be a result of denaturingof the collagen and adjacent muscle fibers. These injured tissues arereinforced and/or replaced by stiff scar tissue. Thickening of thetissue may occur over time, due to stimulation of scar tissue and/orsmooth muscle cell proliferation caused by the tissue injury. Theincrease in modulus may also be the result of tissue shrinkage.Shrinkage of tissues may increase the thickness of the fascial tissueplane, further enhancing the effective increase in modulus of thesupport structure.

The increase in the modulus of elasticity of endopelvic fascia EF has atleast two distinct effects. One effect is to transfer stress from thetarget treatment region 32 to adjoining structures. Stress that wouldnormally be distributed and absorbed as strain throughout the fascialsurface becomes concentrated in the untreated, higher elasticity areas.Hence, if the endopelvic fascia on either side of a fascial tissue planesupporting the urethra is treated and stiffened at locations laterallydisplaced from the urethra (so as to avoid nerve damage to the urethra),the pressure on the fascial plane will result in higher stress on theurethra after treatment.

A second effect of local increases in the modulus is to shorten theresponse time of a structural tissue plane to momentary stress. Thisconcept can be visualized using a simple example: if one were to stop afalling bowling ball with either a steel cable or a rubber band, it isobvious that the stiffer steel cable would stop the ball more quickly.Similarly, treated fascial tissue planes which have been locally orglobally stiffened with scar tissue will stop the decent of the pelvicviscera during a cough much more quickly than untreated, highly elastictissues.

Optional modalities for promoting the growth of scar tissue so as toenhance the modulus of endopelvic fascia EF between first and secondtissues T₁, T₂ include the application of thermal energy (for example,through direct thermal conduction), the application of electrosurgicalenergy, the directing of laser energy (preferably CO₂ laser energy) ontothe fascia, the focusing of ultrasound or microwave energy, or the like.For applying these or other forms of energy to the endopelvic fascia EF,the endopelvic fascia may be accessed surgically, preferably usingminimally invasive surgical techniques so as to apply the energydirectly to a surface of the endopelvic fascia. Alternatively, it may bepossible to direct at least some of these forms of energy through anintervening tissue, as described more fully in co-pending U.S. patentapplication Ser. No. 09/288,865, the full disclosure of which isincorporated herein by reference.

Still further alternative mechanisms for promoting the formation of scartissue so as to enhance the modulus of endopelvic fascia EF include theuse of bioactive agents, such as local drug delivery to target region32, the application of sclerosing agents to harden the tissue (such asabsolute ethanol, silver nitrate, ethanolamine oleate, polidocanol,and/or N-butyl-2-cyanoacrylate), the application of pleurodesis agents,the application of causticcompounds, the use of growth factors, or thedelivery of surgical sealants.

A still further alternative mechanism for increasing the overall supportprovided by the pelvic support system can be understood with referenceto FIGS. 6A-C. As illustrated in FIG. 6A, a first tissue T₁ has a firstendopelvic fascial layer EF1 attached thereto. Similarly, a secondtissue T₂ has a second endopelvic fascial layer EF2, and the secondendopelvic fascial layer is normally free to slide relative to firstendopelvic fascial layer EF1. These fascial planes slide freely withrespect to the adjoining fascial layers to allow the visceral organs toexpand and contract. However, if there is inadequate support for thegenitourinary tract, the motion may become extreme and result in,amongst other conditions, incontinence and/or prolapse.

As illustrated in FIGS. 6B and 6C, joining fascial layers EF1 and EF2reduces the motion available within the pelvic support system, andrestricts movement of the pelvic viscera. The treatment may be targetedto restrict the motion of organs away from their desired supportlocations, for example, by manipulating tissues T₁ and T₂ so that theyare disposed at a desired relative position at the time of attachment.

Several distinct mechanisms are available for attachment of endopelvicfascial layers EF1 and EF2, as can be understood with reference to FIGS.6B and C. As illustrated in FIG. 6B, acute attachment between thefascial layers may be provided by heating the fascial layerssufficiently to fuse the two collagenous tissue planes. In time, achronic healing response to this initial fusing will result in permanentattachment due to the growth of highly cross-linked collagenous tissuespanning the previously separated endopelvic fascial layers, asillustrated in FIG. 6B.

Another chronic response to tissue injury is the development ofsurgically induced adhesions between tissue planes. Adhesions may occureven in locations where acute fusion of planes was not effected. In manycases, thermal damage to the surface of an endopelvic fascial tissueplane is sufficient to stimulate growth of adhesions.

In many pelvic surgeries, prevention of adhesion formation is asignificant goal. Unintended adhesions are generally a source of patientdiscomfort, and may even cause dysfunction. Nonetheless, byintentionally promoting the controlled growth of site-specific adhesionsbetween endopelvic fascial layers EF1 and EF2, the pelvic support systemof the urethra can be significantly enhanced by allowing thetransmission of forces along additional load paths. This can result insignificant patient benefit where adhesions 34 at target location 32serve to support the pelvic viscera, as illustrated in FIG. 6C. Avariety of pleurodesis agents might be applied on, and/or between thefascial layers to cause fibrosis and adhesion formation, includingtalcum, tetracycline and derivatives, bleomycin, sodium hydroxide,blood, mitomycin, doxycycline, mitoxatrone, and/or dilute acids.Adhesion formation may also be promoted by the application of otherbioactive agents described herein, by direct or remote transmission ofenergy, by mechanical trauma, or by combinations of these techniques.

Fascial layers EF1 and EF2 may comprise a variety of tissue structures,as generally described above. Suitable fascial layers which might beattached together so as to enhance structural support and inhibitincontinence include the periurethral fascia and the levator fascia.

Probe 28 of the system of FIG. 10 is illustrated in more detail in FIG.7A, while methods for its use can be understood with reference to FIGS.7B and 7C. Probe 28 includes an array of electrode pairs 36 mounted to aprobe body 38. Probe body 38 may optionally be supported on a shaft 40,which will typically contain the wires coupling electrode pairs 36 topower supply 26 (see FIG. 1). Electrode pairs 36 are selectivelyenergized by the processor of system 10, so as to transmit sufficientenergy to the endopelvic fascia to effect the desired treatment. Hence,processor 20 can tailor the treatment for a specific patient'sdiagnosis, for example, by varying the area of target region 32 so as tostiffen the endopelvic fascia layer sufficiently to maintain theurethral pressure above the vesicular pressure throughout a pressurepulse.

As explained in more detail in application Ser. No. 09/170,767 case,electrodes 36 indirectly engage surface S of endopelvic fascia EF oneither side of urethra U. Optionally, the probe may include temperaturesensors so as to provide a feedback signal FS to processor 20 so as tomaintain the temperature of the endopelvic fascia within a targettemperature range. Optionally, the target temperature range may besufficient to promote scar tissue formation and/or attachment of theendopelvic fascial layer, and may be insufficient to induce shrinkage ofthe endopelvic fascia. Alternatively, both scar tissue formation andshrinkage may be effected simultaneously. Preferably, probe 28 is usedin a static position so that the treatment area is controlled byprocessor 20 via switching unit 29 selectively applying power to some orall of electrode pairs 36, the number and location of electrode pairs,the heat time, and the heat temperature being sufficient to achieve thedesired result. FIG. 7B illustrates an optional method for accessingsurface S of endopelvic fascia EF transvaginally, by displacing a flap Ffrom the vaginal wall VW with the assistance of a weighted speculum 40.

A laparoscopic device and method for directly heating endopelvic fasciaEF can be understood with reference to FIG. 8A and B. Laparoscopic probe42 includes a shaft 44 supporting an electrode pair 36 relative tohandle 46. A variety of electrode pair configurations might be used, asmore fully described in co-pending U.S. patent application Ser. No.08/910,370. Preferably, a port 48 will be disposed adjacent and/orbetween electrodes 36 to allow a small amount of irrigation flow beforeand/or during the treatment. This irrigation flow may comprise aconductive fluid such as saline or a non-conductive fluid, and willideally be sufficient to avoid the accumulation of residue on theelectrode pair surfaces. Suitable flow rates will often be in a rangefrom about 0.5 cc/min. to about 10.0 cc/min.

Laparoscopic probe 42 will generally be used in a laparoscopic procedureusing a superior approach, typically under the direction of alaparoscope 50 inserted near the patient's mid-line (for example,adjacent the belly button). Handle 46 is manipulated so as to “paint”bipolar electrode 36 across the endopelvic fascia surface until thetarget region has been sufficiently heated.

FIG. 9 illustrates a still further alternative probe for use with thesystem of FIG. 1. In this embodiment, a transvaginal bipolar probe 54includes an electrode pair 36 which is cooled by fluid conduits 56. Thefluid conduits cool the intervening tissue between bipolar probe 54 andendopelvic fascia EF via electrodes 36, and via the probe surfacebetween the electrodes. Similarly, the tissue disposed beyond theendopelvic fascia (in this case a wall of bladder B) is cooled, here bycirculation of a cooled solution within the bladder. Once theintervening tissue of the vaginal wall VW (and the bladder B beyond thetarget region of endopelvic fascia EF) are cooled sufficiently, RFcurrent is transmitted between the electrodes to heat the endopelvicfascia. Advantageously, the pre-cooling can redirect the current flux 58from the intervening and adjacent tissues to a desired flux pattern 60.Feedback on the pre-cooling and heating temperatures may be provided byneedle-mounted temperature sensors 62 mounted to the probe, and/or bytemperature sensors mounted to the probe surface.

Referring now to FIG. 10, pressuregram 22 is illustrated in more detail.Generally, a patient will remain continent so long as urethral pressureP_(u) remains higher than vesicular pressure P_(v). Pressuregram 22traces the changes in urethral and vesicular pressure during a pressurepulse, such as during a cough. For patient “A”, the trace of thesepressures throughout the pressure pulse or pulses remains above a lineindicating the pressures are equal, so that patient “A” has remainedcontinent throughout the stress event. In fact, the slope of thepressuregram appears to be at or above unity, so that it appears thatpatient “A” will remain continent for larger pressure pulses.

The pressuregram of patient “B” does not remain above the P_(u)=P_(v)line. Hence, at some point during the pressure pulse, the vesicularpressure is greater than the urethral pressure, and leakage may occur.To increase the slope of pressuregram trace for patient “B”, the supportprovided by the patient's pelvic support system may be enhanced asdescribed hereinabove. Optionally, the modulus of elasticity of one ormore of the support tissues may be enhanced by promoting scar tissueformation. This will increase the slope of patient “B's” pressure pulsetrace. The support tissue may, either alternatively or in combinationwith modulus changes, be enhanced by attaching adjacent tissue planestogether, or by selectively shrinking support tissues. These lattertreatments may increase the urethral pressure relative to the vesicularpressure, moving the pressuregram pulse trace farther from the unityline.

Advantageously, the treatment of the present invention may be tailoredbased on the pressuregram of a particular patient. For example, scartissue formation may be modulated based on the desired increase inpressuregram pulse slope for a particular patient by varying the areatreated and/or amount of treatment (and hence scar tissue formation) fora given area, with increasing changes in pressuregram slope generallyprovided by increasing treatment quantity. Similarly, selectiveshrinking may help increase the height of the pressuregram pulse traceabove the unity line (at which urethral and vesicular pressures areequal).

Referring now to FIG. 11, a kit 70 for treating incontinence includeslaparoscopic probe 42 and instructions for its use 72 within packaging74. Kit 70 may include any of the probes described hereinabove, whileinstructions for use 72 will generally describe method steps foreffecting any of the methods of the present invention. Packaging 74 maycomprise a sterile package, and/or probe 42 may be separately packagedin a sterile container within kit 70. Instructions for use 72 may be atleast in part disposed on packaging 74 or packaging for probe 42, andthe instructions may be in the form of a tangible machine readable codeor analog information such as a computer disk, a video tape, a CD ROM,or the like.

While the exemplary embodiments of the present invention have beendescribed in some detail, by way of example and for clarity ofunderstanding, a variety of changes, modifications, and adaptations willbe obvious to those of skill in the art. Hence, the scope of the presentinvention is limited solely by the appended claims.

What is claimed is:
 1. A system to treat incontinence of a patient, thepatient having a collagenous support tissue supporting a urethra and,prior to treatment, exhibiting leakage resulting from anincontinence-event stress pulse, the system comprising: a probe fordelivering energy or an active agent to the support tissue so as toinduce a healing response in the support tissue, the healing responsereducing an elasticity of the support tissue; and a control systemcoupled to the probe, the control system directing the delivery from theprobe so that the reduction of elasticity of the support tissue inhibitsmovement of the urethra during the stress pulse, the control systemlimiting the amount of the energy or the agent to avoid shrinkage of thetissue.
 2. The system of claim 1, wherein the probe comprises an energydelivery member.
 3. The system of claim 1, further comprising: aurethral pressure sensor; a vesicle pressure sensor; a processor coupledto the urethral pressure sensor and the vesicle pressure sensor, theprocessor generating an output indicating a change in urethral pressurerelative to a change in vesicle pressure, the control system directingthe delivery in response to the output from the processor.
 4. The systemof claim 2, wherein the energy delivery member comprises an electrode.5. A kit for treating incontinence, the kit comprising: the system ofclaim 1; and instructions for using the probe to enhance structuralsupport provided by the support tissue so as to inhibit movement of theurethra from the incontinence-event stress pulse so that incontinence isinhibited.
 6. A system to treat incontinence of a patient, the patienthaving a collagenous support tissue supporting a urethra and, prior totreatment, exhibiting leakage resulting from an incontinence-eventstress pulse, the system comprising: a probe for delivering energy or anactive agent to the support tissue so as to reduce an elasticity of thesupport tissue; a control system coupled to the probe, the controlsystem directing the delivery from the probe so that the reduction ofelasticity of the support tissue inhibits movement of the urethra duringthe stress pulse; a urethral pressure sensor; a vesicle pressure sensor;a processor coupled to the urethral pressure sensor and the vesiclepressure sensor, the processor generating an output indicating a changein urethral pressure relative to a change in vesicle pressure, thecontrol system directing the delivery in response to the output from theprocessor.
 7. A system to treat incontinence of a patient, the patienthaving a collagenous tissue coupled to a urethra and, prior totreatment, exhibiting leakage resulting from an incontinence-eventstress pulse, the system comprising: a probe for delivering energy tothe tissue so as to induce a healing response in the tissue, the healingresponse reducing an elasticity of the tissue; and a control systemcoupled to the probe, the control system directing the delivery from theprobe so that the reduction of elasticity of the tissue inhibits leakagethrough the urethra during the stress pulse, the control system limitingthe amount of the energy to avoid shrinkage of the tissue.